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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Molecular biological findings have indicated that the affinity and the density of presynaptic serotonin transporters may be subject to adaptive regulation, but the physiological conditions that may act to trigger such changes are presently unknown. By means of [3H]paroxetine binding to rat cortical membranes, we studied the influence of two physiological variables that are clearly associated with altered serotonergic activity—circadian rhythm and semistarvation—on KD and Bmax values of the serotonin transporter of the rat frontal cortex. No circadian fluctuations of both parameters were observed. Also, semistarvation (50% reduction of normal voluntary food intake) for 2 days had no effect on either KD or Bmax values of cortical [3H]paroxetine binding. Food restriction for either 7 days or 2 weeks, however, resulted in a significant, ∼30%, reduction of the density of cortical serotonin transporters with unchanged transporter affinity. These findings indicate that long-term changes in the density of cortical serotonin transporters can be induced by long-lasting alterations of certain environmental variables. Because the duration and the radius of action of presynaptically released serotonin are governed by the efficiency of the reuptake mechanism, such adaptive changes of serotonin transporter density must be expected to cause long-term alterations of the modulatory impact of the central serotonin system on certain brain functions.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of pineal research 19 (1995), S. 0 
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Polysomnographic sleep patterns and melatonin secretion were investigated in 10 patients (age: 41.3 ± 9.5 years) who suffered from chronic primary insomnia and complained predominantly about difficulties in maintaining sleep and in five healthy controls (age 27.2 ± 0.7 years). Nocturnal plasma melatonin concentrations were obtained hourly, measured by direct radioimmunoassay and statistically compared between insomniacs and controls with age as a covariate. Plasma melatonin levels in the patient group tended to begin increasing earlier in the evening and were significantly (P ± 0.01) lower during the middle of the night (peak value 82.5 ± 26.5 pg/ml) than in the healthy controls (peak value 116.8 ± 13.5 pg/ml). Among the patients, the most severely reduced nocturnal plasma melatonin levels were found in those patients with a history of sleep disturbance lasting for longer than five years (N = 6; age 41.8 ± 11.7 years; duration 15.3 ± 5.9 years; peak value 72.1 ± 25.0 pg/ml); whereas those chronic insomniacs affected for fewer than five years had relatively higher nocturnal levels (N = 4; age 40.6 ± 6.5 years; duration 3.8 ± 1.5 years; peak value 98.2 ± 23.9 pg/ml). These results show that the circadian rhythm of melatonin secretion is disturbed in patients with chronic primary insomnia, and that the nocturnal plasma melatonin secretion is increasingly more affected the longer the patients are unable to maintain a regular sleep pattern.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of pineal research 25 (1998), S. 0 
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Rodenbeck A, Huether G, Rüther E, Hajak G. Altered circadian melatonin secretion patterns in relation to sleep in patients with chronic sleep-wake rhythm disorders. J. Pineal Res. 1998; 25:201–210. © Munksgaard, Copenhagen〈section xml:id="abs1-1"〉〈title type="main"〉AbstractHuman well-being depends on the entrainment of endogenous circadian rhythms of biological functions and the sleep-wake rhythm. Although the incidence of otherwise healthy subjects with chronically altered sleep-wake rhythms is rather low, the investigation of these patients provides new sights into circadian entrainment mechanisms. We therefore examined the circadian rhythm of circulating melatonin and the sleep-wake rhythm in five patients with chronic sleep-wake rhythm disorders and ten age-matched healthy controls. All patients showed altered circadian melatonin rhythm parameters in relation to their sleep-wake cycle compared to age-matched controls. These alterations were random, i.e., independent of the type, the duration, and the age of onset of the disorder. The melatonin onset to sleep onset interval varied between the patients and the melatonin acrophase to sleep offset interval was prolonged in four patients. These findings indicate individual phase relations between the circadian melatonin rhythm and the sleep-wake cycle in patients with chronic sleep-wake rhythm disorders. Since the prolonged melatonin acrophase to sleep offset interval was the most consistent finding independent of aetiological origins, this abnormality may be one possible maintaining factor in chronic sleep-wake rhythm disorders due to reduced phase-resetting properties of the circadian pacemaker. Furthermore, rather low circadian melatonin amplitudes and a subsensitivity to daylight may maintain the disorder in at least some patients.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1433-8491
    Keywords: Memory disorders ; Dementia ; Depression ; Diagnosis ; Primary care
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate whether an early diagnosis of dementia is established, whether a differentiation is made between vascular and primary degenerative etiology, and whether treatable causes of dementia are considered in primary care, we performed a survey using three written sample case histories describing slight memory impairment (case 1) or moderate dementia (case 2a: vascular dementia; case 2b: degenerative dementia of Alzheimer type). The combinations 1 and 2a or 1 and 2b were randomly assigned and presented to ambulatory-care physicians (145 general practitioners and primary care internists and 14 neuropsychiatrists in private practice) in Göttingen and rural surroundings by a trained investigator who then performed a standardized interview. The study was representative (response rate 83.2%). For the sample case with slight memory complaints 13.8% of all physicians arrived at a primary diagnosis of depression and 44.0% considered depression for differential diagnosis. Senile dementia of Alzheimer type was considered less often. In the sample cases with moderate dementia according to established scientific criteria, there was a striking under-diagnosis of dementia, and in both cases an over-diagnosis of underlying vascular etiology. Treatable causes of dementia, such as possible drug interactions and substance abuse, were considered only by a minority of physicians. In conclusion, memory deficits seem to be regarded mainly as consequences of disturbed cerebral perfusion, and dementia as well as depression and drug adverse effects seem to be under-diagnosed in primary care.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 246 (1996), S. 79-82 
    ISSN: 1433-8491
    Keywords: Rebound insomnia ; Withdrawal symptoms ; Clozapine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rebound insomnia has been reported upon discontinuation of benzodiazepines. We describe the first case of a sleep polygraphically documented rebound insomnia with an unusual somatic fatigue syndrome after long-term use of clozapine in a 30-year-old schizophrenic male. The withdrawal symptoms occurred the first day after drug discontinuation and could be stopped by readministering clozapine. In our opinion, the sudden occurrence of the withdrawal symptoms cannot be explained by a dopaminergic hypersensitivityor a cholinergic rebound, but indicates an involvement of GABAergic and perhaps antiglutamatergic properties of clozapine.
    Type of Medium: Electronic Resource
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